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Updated: Feb 19, 2026
Experimental and Imaging Techniques for Examining Fibrin Clot Structures in Normal and Diseased States
Published on: April 1, 2015
[Diabetes Mellitus, a prothrombotic disease]
F Picard1, J Adjedj1, O Varenne1
1Interventional cardiology department, Cochin hospital, Assistance publique-Hôpitaux de Paris, 27, rue du Faubourg-Saint-Jacques, 75014 Paris, France; Université Paris Descartes, université Sorbonne Paris Cité, 75006 Paris, France.
Insights
Diabetes significantly increases thrombotic risk due to hyperglycemia and hyperinsulinism, contributing to atherothrombotic events. Understanding these prothrombotic mechanisms is crucial for managing cardiovascular complications in diabetic patients.
Area of Science:
- Cardiovascular Science
- Endocrinology
- Hematology
Background:
- Diabetes mellitus is a growing global health concern, affecting over 500 million people.
- Diabetic patients frequently experience atherothrombotic disease, with cardiovascular events remaining a leading cause of mortality.
- Despite advances, the molecular links between diabetes and increased thrombogenicity are not fully understood.
Purpose of the Study:
- To review the prothrombotic nature of diabetes.
- To update knowledge on the cellular and molecular mechanisms driving thrombogenicity in diabetes.
- To discuss the therapeutic implications of the prothrombotic state in diabetic patients.
Main Methods:
- Literature review focusing on cellular and molecular mechanisms.
- Analysis of factors contributing to hypercoagulability in diabetes.
- Examination of impaired fibrinolysis and platelet function in diabetic conditions.
Main Results:
- Type 1 and Type 2 diabetes are characterized by a prothrombotic state driven by hyperglycemia and hyperinsulinism.
- Increased procoagulant factors, tissue factor, and microparticle involvement contribute to thrombogenicity.
- Impaired fibrinolysis, platelet hyperreactivity, endothelial dysfunction, and inflammation exacerbate the prothrombotic condition.
Conclusions:
- Diabetes significantly elevates thrombotic risk through multiple interconnected pathways.
- Understanding these mechanisms is vital for developing effective therapeutic strategies for diabetic cardiovascular complications.
- Further research into the cellular and molecular basis of diabetes-associated thrombogenicity is warranted.
Abstract:
In patients with acute atherothrombotic disease, diabetes or glucose intolerance is frequently found. Indeed, the number of people with diabetes in the world continues to increase and is expected to reach more than 500 million people by 2035. Diabetes is a pathology commonly associated with both microvascular and macrovascular complications. Although the mortality of coronary artery disease has decreased significantly over the past 20 years, mortality in patients with type 2 diabetes has changed little and atherothrombotic events remain the leading cause of death in diabetic patients. Although our understanding of vascular pathology has greatly evolved in recent years, the cellular and molecular mechanisms linking thrombogenicity and diabetes remain incompletely understood. Type 1 and type 2 diabetes are prothrombotic pathologies. This prothrombotic state is due to both hyperglycemia and chronic hyperinsulinism. Among the different agonists involved in the increased thrombogenicity of diabetic patients, abnormalities can be found in all phases of coagulation. Increased procoagulant factors and tissue factor associated with impaired fibrinolysis, platelet hyperreactivity, endothelial dysfunction, leukocyte activation, low-grade inflammation, and microparticle involvement, they all play a role in the establishment of this prothrombotic condition. This review sought to provide an update on the prothrombotic nature of diabetes and its consequences in therapeutics.
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